Version May 2024
Elevated intraocular pressure: Ophthalmic:
Solution: Instill 1 to 2 drops into affected eye(s) twice daily.
Suspension (Betoptic S): Instill 1 drop into affected eye(s) twice daily.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
Refer to adult dosing.
(For additional information see "Betaxolol (ophthalmic): Pediatric drug information")
Elevated intraocular pressure: Infants, Children, and Adolescents: Ophthalmic suspension (Betoptic S): Instill 1 drop into affected eye(s) twice daily
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Infants, Children, and Adolescents: There are no dosage adjustments provided in manufacturer's labeling (has not been studied).
Infants, Children, and Adolescents: There are no dosage adjustments provided in manufacturer's labeling (has not been studied).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Frequency not always defined.
Ophthalmic: Eye discomfort (≤25%; short-term), anisocoria, blurred vision, choroidal detachment, corneal staining, crusting of eyelash, decreased corneal sensitivity, decreased visual acuity, eye discharge, eye pain, eye pruritus, eye redness, foreign body sensation of eye, hypersensitivity reaction (ophthalmic), keratitis, lacrimation, ocular edema, ophthalmic inflammation, photophobia, punctate corneal staining (with or without dendritic formations), superficial punctate keratitis, xerophthalmia
<1%, postmarketing, and/or case reports: Alopecia, altered sense of smell, asthma, bradycardia, bronchospasm, cardiac failure, depression, dizziness, dysgeusia, dyspnea, exacerbation of myasthenia gravis, glossitis, heart block, headache, insomnia, lethargy, respiratory failure, thickening of bronchial secretions, toxic epidermal necrolysis, urticaria, vertigo
Hypersensitivity to betaxolol or any component of the formulation; sinus bradycardia; atrioventricular block greater than first-degree; cardiogenic shock; uncompensated cardiac failure.
Canadian labeling: Additional contraindications (not in US labeling): Reactive airway disease including bronchial asthma or a history of bronchial asthma; severe chronic obstructive pulmonary disease (COPD); sick sinus syndrome sino-atrial block
Concerns related to adverse events:
• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
Disease-related concerns:
• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring; asthma exacerbation and pulmonary distress has been reported during betaxolol use.
• Cardiovascular insufficiency: Use with caution in patients with cardiovascular insufficiency; if signs of decreased cerebral blood flow occur, consider alternative therapy.
• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
• Heart failure: Use with caution in patients with compensated heart failure (HF) and monitor for a worsening of the condition. Discontinue at the first signs of cardiac failure. In a scientific statement from the American Heart Association, betaxolol has been determined to be an agent that may exacerbate underlying myocardial dysfunction (magnitude: major) (AHA [Page 2016]).
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; may worsen disease.
• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.
• Vascular insufficiency: Use with caution in patients with vascular insufficiency due to potential effects on blood pressure and pulse; if signs/symptoms of reduced cerebral blood flow or Raynaud phenomenon (RP) develop during therapy, consider alternative therapy.
Special populations:
• Contact lens wearers: Ophthalmic solution/suspension contains benzalkonium chloride which may be absorbed by contact lenses; remove contact lens prior to administration and wait 15 minutes before reinserting.
Dosage form specific issues:
• Ophthalmic: Inadvertent contamination of multiple-dose ophthalmic solutions has caused bacterial keratitis. Should not be used alone in angle-closure glaucoma (has no effect on pupillary constriction). Choroidal detachment has been reported with aqueous suppressant therapy after filtration procedures.
Other warnings/precautions:
• Absorption: Systemic absorption of betaxolol and adverse effects may occur with ophthalmic use, including severe respiratory and cardiac reactions.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Ophthalmic:
Generic: 0.5% (5 mL, 10 mL, 15 mL)
Suspension, Ophthalmic:
Betoptic-S: 0.25% (10 mL [DSC], 15 mL [DSC])
Betoptic-S: 0.25% (10 mL, 15 mL) [contains benzalkonium chloride, edetate (edta) disodium]
May be product dependent
Solution (Betaxolol HCl Ophthalmic)
0.5% (per mL): $12.33
Suspension (Betoptic-S Ophthalmic)
0.25% (per mL): $44.29
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Suspension, Ophthalmic:
Betoptic-S: 0.25% (5 mL, 10 mL) [contains benzalkonium chloride, edetate (edta) disodium]
Ophthalmic: Shake suspension well before using. Tilt head back and instill in eye. Keep eye open and do not blink for 30 seconds. Apply gentle pressure to lacrimal sac for 1 minute. Wipe away excess from skin. Do not touch applicator to eye and do not contaminate tip of applicator. Administer other ophthalmic agents at least 10 minutes prior to instilling betaxolol products.
Ophthalmic: Administer other topically applied ophthalmic medications at least 10 minutes before Betoptic S; wash hands before use; shake well before administration; do not allow the dispenser tip to touch the eye. Apply gentle pressure to lacrimal sac during and immediately following instillation (1 minute) or instruct patient to gently close eyelid after administration to decrease systemic absorption of ophthalmic drops (Ref). Some solutions contain benzalkonium chloride; wait at least 15 minutes after instilling solution before inserting soft contact lenses.
Elevated intraocular pressure: Treatment of elevated intraocular pressure in patients with chronic open-angle glaucoma or ocular hypertension.
Betoptic S may be confused with Betagan, Timoptic
Substrate of CYP1A2 (minor), CYP2D6 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider therapy modification
Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Risk C: Monitor therapy
Antidiabetic Agents: Beta-Blockers (Beta1 Selective) may enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Antipsychotic Agents (Phenothiazines): May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. Risk C: Monitor therapy
Beta2-Agonists: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Beta2-Agonists. Of particular concern with nonselective beta-blockers or higher doses of the beta1 selective beta-blockers. Risk C: Monitor therapy
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Cannabis: Beta-Blockers may enhance the adverse/toxic effect of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification
Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor therapy
Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy
Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Risk C: Monitor therapy
DOBUTamine: Beta-Blockers may diminish the therapeutic effect of DOBUTamine. Risk C: Monitor therapy
Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider therapy modification
EPHEDrine (Systemic): Beta-Blockers may diminish the therapeutic effect of EPHEDrine (Systemic). Risk C: Monitor therapy
EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Nasal). Risk C: Monitor therapy
EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Risk C: Monitor therapy
Epinephrine (Racemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of Epinephrine (Racemic). Risk C: Monitor therapy
EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Systemic). Risk C: Monitor therapy
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor therapy
Etilefrine: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may diminish the therapeutic effect of Etilefrine. Risk C: Monitor therapy
Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Risk X: Avoid combination
Etrasimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider therapy modification
Isoproterenol: Beta-Blockers may diminish the therapeutic effect of Isoproterenol. Risk C: Monitor therapy
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Mavacamten: Beta-Blockers may enhance the adverse/toxic effect of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor therapy
Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Risk C: Monitor therapy
Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Mivacurium: Beta-Blockers may enhance the therapeutic effect of Mivacurium. Risk C: Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Risk C: Monitor therapy
Nitrendipine: May enhance the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Reserpine: May enhance the bradycardic effect of Beta-Blockers. Reserpine may enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Risk X: Avoid combination
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification
Succinylcholine: Beta-Blockers may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Tasimelteon: Beta-Blockers may diminish the therapeutic effect of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider therapy modification
Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Theophylline Derivatives. Risk C: Monitor therapy
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
White Birch Allergen Extract: Beta-Blockers may enhance the adverse/toxic effect of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid combination
When administered orally, betaxolol crosses the placenta and can be detected in the amniotic fluid and umbilical cord blood (Morselli 1990).
The amount of betaxolol available systemically following topical application of the ophthalmic drops is significantly less in comparison to oral doses (Vainio-Jylhä 2001). However, the same adverse effects observed with systemic administration may occur. If ophthalmic agents are needed during pregnancy, the minimum effective dose should be used in combination with punctal occlusion to decrease potential exposure to the fetus (Johnson 2001; Salim 2014; Samples 1988).
It is not known if betaxolol is present in breast milk following ophthalmic administration.
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. The minimum effective dose should be used in combination with punctual occlusion to decrease potential exposure to the breastfeeding infant (Johnson 2001; Salim 2014; Samples 1988).
Intraocular pressure
Competitively blocks beta1-receptors, with little or no effect on beta2-receptors; with ophthalmic use, reduces intraocular pressure by reducing the production of aqueous humor
Onset of action: Within 30 minutes
Peak effect: Intraocular pressure reduction: ~2 hours
Duration: ≥12 hours
Absorption: Rapidly absorbed into the systemic circulation (concentrations ~1/10 to 1/20 of oral dosing) (Vainio-Jylhä, 2001)
Excretion: Urine (>80%, as unchanged drug [15%] and inactive metabolites)
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